The rat will be used as a model animal to study the ontogeny of feeding controls during the suckling and weanling periods. Preliminary evidence suggests that, whilst satiety may be present from birth onwards, hunger may not appear until the third postnatal week, which is when the rat pup begins to wean. Further studies are needed to verify these developmental time courses and to establish the physiological and biochemical bases of hunger and satiety in the infant animal. Hunger will be assessed by studying feeding latencies of fed and fasted animals. Manipulations that are known to elicit hunger in the adult will be investigated at various stages of infancy. The aim will be to assess whether the hunger mechanism has the same physiology from its outset as in adulthood. Specifically, the possibility of glucostatic, lipostatic, thermostatic and lateral hypothalamic control of infant hunger will be studied. Since current evidence suggests that there is a temporal correlation between the ontogenic appearance of hunger and the beginning of the process of weaning, the possibility of a causal relationship between these two phenomena will be investigated. The developmental time course of satiety will be determined using the parameter of meal size, as indicated by weight gain during a 4 hr. feeding period. Possible mediation of satiety by gastrointestinal distension, the duodenal hormone cholecystokinin and absorbed glucose, will be investigated. The influence of endocrine, dietary and genetic factors on the ontogeny of hunger and satiety will be determined. With respect to endocrine control, particular attention will be given to thyroid and glucocorticoid hormones. The major dietary study will be to determine whether the administration of highly palatable foods during the suckling period interferes with the ontogeny of feeding controls in such a way as to predispose infants to adult obesity. Finally, the ontogeny of hunger and satiety will be studied in genetically obese rats (Zucker) so as to determine whether abnormal development of feeding controls plays a role in the expression of the obese phenotype.